Does depression help people do art? Does autism help people do science? Does the normal mind without enough of either come up short in creativity? Not sure. But relatives of those with depression have different intellectual interests than relatives of those who have autism.

A hallmark of the individual is the cultivation of personal interests, but for some people, their intellectual pursuits might actually be genetically predetermined. Survey results published by Princeton University researchers in the journal PLoS ONE suggest that a family history of psychiatric conditions such as autism and depression could influence the subjects a person finds engaging.

Although preliminary, the findings provide a new look at the oft-studied link between psychiatric conditions and aptitude in the arts or sciences. While previous studies have explored this link by focusing on highly creative individuals or a person's occupation, the Princeton research indicates that the influence of familial neuropsychiatric traits on personal interests is apparently independent of a person's talent or career path, and could help form a person's basic preferences and personality.

Princeton researchers surveyed nearly 1,100 students from the University's Class of 2014 early in their freshman year to learn which major they would choose based on their intellectual interests. The students were then asked to indicate the incidence of mood disorders, substance abuse or autism spectrum disorder (ASD) in their family, including parents, siblings and grandparents.

Students interested in pursuing a major in the humanities or social sciences were twice as likely to report that a family member had a mood disorder or a problem with substance abuse. Students with an interest in science and technical majors, on the other hand, were three times more likely to report a sibling with an ASD, a range of developmental disorders that includes autism and Asperger syndrome.

I suspect moderate doses of genes for autism make the mind much more capable of handling the rigor required to do math and science. The "normal" human mind is not as well suited to understand the world scientifically.

What I wonder: does maladaptive autism exist further out on a spectrum from adaptive autistic traits? Or is maladaptive autism caused by other genetic variants beyond those that cause more adaptive forms of altruism?

Here's the abstract and full paper.

From personality to neuropsychiatric disorders, individual differences in brain function are known to have a strong heritable component. Here we report that between close relatives, a variety of neuropsychiatric disorders covary strongly with intellectual interests. We surveyed an entire class of high-functioning young adults at an elite university for prospective major, familial incidence of neuropsychiatric disorders, and demographic and attitudinal questions. Students aspiring to technical majors (science/mathematics/engineering) were more likely than other students to report a sibling with an autism spectrum disorder (p = 0.037). Conversely, students interested in the humanities were more likely to report a family member with major depressive disorder (p = 8.8×10⁻⁴), bipolar disorder (p = 0.027), or substance abuse problems (p = 1.9×10⁻⁶). A combined PREdisposition for Subject MattEr (PRESUME) score based on these disorders was strongly predictive of subject matter interests (p = 9.6×10⁻⁸). Our results suggest that shared genetic (and perhaps environmental) factors may both predispose for heritable neuropsychiatric disorders and influence the development of intellectual interests.

Since genetic sequencing costs have crashed over the the last decade and especially in the last few years we are about to get the flood of DNA sequencing data needed to identify large numbers of genetic variants that contribute to cognitive traits. The picture will be much much clearer in just 4 or 5 years. I'm awaiting the discoveries with great interest.

Before car computers totally take over the task of driving they will continue to gain more capabilities for accident avoidance. The latest: use of wireless technology so that car computers can know distances and velocity and collision risk of nearby cars.

Vehicle-to-vehicle communication—known as "V2V" in the industry—is eagerly anticipated because it could help reduce crashes. The Wi-Fi signals, which go out in all directions, would act like an alert passenger, warning the driver that another car is about to run a red light or that there's a motorcycle in the blind spot. U.S. government researchers estimate that V2V would let drivers avoid or make less serious around 80 percent of collisions.

Just like anti-lock brakes (ABS) and other car risk reduction technologies anything that works well enough will eventually become mandated by regulatory agencies. So perhaps in 10 or 15 years cars will all come with WiFi transmitters and receivers that work to detect dangerous approaches between cars.

One can imagine street lights continuously broadcasting not just their current settings but also when they will change. This will enable better calculations of collision risks.

I expect another benefit: cars approaching a street light will signal asking for a green. If the street light doesn't get similar signals from the cross street it will change to give the green to the approaching car. Newer cars would then again an advantage in getting thru street lights.

Rising atmospheric carbon dioxide might cause so much heating that some countries will respond by releasing sulfate aerosols to reflect sunlight and cool the planet. If that happens the question arises: Will the net effect of less sunlight (which would reduce energy flowing to plants) be outweighed by the plant-boosting effects of lower temperatures and higher CO2? Some climate scientists did modeling that suggests globally crop yields would rise overall but fall in some areas.

Although scientists know that climate change in recent decades has negatively impacted crop yields in many regions, the study by Pongratz and colleagues is the first to examine the potential effect of geoengineering on food security. Pongratz's team, which included Carnegie's Ken Caldeira and Long Cao, as well as Stanford University's David Lobell, used models to assess the impact of sunshade geoengineering on crop yields.

Using two different climate models, they simulated climates with carbon dioxide levels similar to what exists today. A second set of simulations doubled carbon-dioxide levels – levels that could be reached in several decades if current trends in fossil-fuel burning continue unabated. A third set of simulations posited doubled carbon dioxide, but with a layer of sulfate aerosols in the stratosphere deflecting about 2% of incoming sunlight away from the Earth. The simulated climate changes were then applied to crop models that are commonly used to project future yields.

The team found that, in the model, sunshade geoengineering leads to increased crop yields in most regions, both compared with current conditions and with the future projection of doubled carbon dioxide on its own. This is because deflecting sunlight back to space reduces temperatures, but not CO2. "In many regions, future climate change is predicted to put crops under temperature stress, reducing yields. This stress is alleviated by geoengineering," Pongratz said. "At the same time, the beneficial effects that a higher CO2 concentration has on plant productivity remain active."

Of course this work was done with a model that is much simpler than the real planet. Future improvements in model quality could yield different results. Still, an interesting result.

The researchers point out that sulfate aerosols would not reverse the ocean acidification caused by more CO2 dissolving into the oceans. Speaking of ocean acidification, rising atmospheric CO2 will increase the acidification of the oceans so much that the coral reefs would drastically shrink in extent.

"In some regions, the man-made rate of change in ocean acidity since the Industrial Revolution is hundred times greater than the natural rate of change between the Last Glacial Maximum and pre-industrial times," emphasizes Friedrich. "When Earth started to warm 17,000 years ago, terminating the last glacial period, atmospheric CO2 levels rose from 190 parts per million (ppm) to 280 ppm over 6,000 years. Marine ecosystems had ample time to adjust. Now, for a similar rise in CO2 concentration to the present level of 392 ppm, the adjustment time is reduced to only 100 – 200 years."

On a global scale, coral reefs are currently found in places where open-ocean aragonite saturation reaches levels of 3.5 or higher. Such conditions exist today in about 50% of the ocean – mostly in the tropics. By end of the 21st century this fraction is projected to be less than 5%. The Hawaiian Islands, which sit just on the northern edge of the tropics, will be one of the first to feel the impact.

If necessary we could use a variety of climate engineering techniques to prevent the melting of Antarctica and Greenland. But I've yet to come across a proposal for how to prevent a shift in ocean acidity as atmospheric CO2 continues to rise.

Why not a higher autism correlation between twins? birth weight is a key factor in determining autism risk.

EVANSTON --- Although the genetic basis of autism is now well established, a growing body of research also suggests that environmental factors may play a role in this serious developmental disorder affecting nearly one in 100 children. Using a unique study design, a new study suggests that low birth weight is an important environmental factor contributing to the risk of autism spectrum disorder (ASD).

“Our study of discordant twins -- twin pairs in which only one twin was affected by ASD -- found birth weight to be a very strong predictor of autism spectrum disorder,” said Northwestern University researcher Molly Losh. Losh, who teaches and conducts research in Northwestern’s School of Communication, is lead author of the study that will be published in the journal “Psychological Medicine” and is now available online.

But let me quibble about terminology: For millions of people on the autistic spectrum their autistic minds are not a disorder. Many are quite high functioning and happy to be on the autistic spectrum with the intellectual advantages they gain from their modes of thought. I think the problem is that too much cognitive variation has gotten subsumed under the autism label.

Still, this finding on birth weight is important.

The researchers found that lower birth weight more than tripled the risk for autism spectrum disorder in identical twin pairs in which one twin had ASD and the other did not.

My guess (and I expect this to become crystal clear in under 10 years due to cheap DNA sequencing technology) is that many genes that cause some aspects of autism were selected for. There was an adaptive advantage to a sort of specialization of cognitive labor. Genetic influences on a phenomenon that occurs a fairly high rate of incidence usually point to something that was selected for rather than developmental error or relatively rarer purely harmful genetic mutations. Highly maladaptive traits rarely get selected for.

There's some overlap between autism as a result of genes selected due to their reproductive advantages versus events that go wrong in brain development. That overlap has made clear thinking about autism harder to do. Given that clear thinking about the mind is hard to do in general that's not too surprising. But on the bright side, advances in psychometrics, neuroscience, and genetics are going to usher in a new age of understanding of the human mind and along with it will come a much more nuanced view of autism.

Some happy old lab mice have been able to resume reading in lower light conditions.

Researchers funded by the Biotechnology and Biological Sciences Research Council (BBSRC) have found that vitamin D reduces the effects of ageing in mouse eyes and improves the vision of older mice significantly. The researchers hope that this might mean that vitamin D supplements could provide a simple and effective way to combat age-related eye diseases, such as macular degeneration (AMD), in people.

The research was carried out by a team from the Institute of Ophthalmology at University College London and is published in the current issue of the journal Neurobiology of Ageing.

The retina's cells are very heavy energy users, heavier energy users than any other cell type in the body. I did not know that.

Professor Glen Jeffery, who led the work, explains "In the back of the eyes of mammals, like mice and humans, is a layer of tissue called the retina. Cells in the retina detect light as it comes into the eyes and then send messages to the brain, which is how we see. This is a demanding job, and the retina actually requires proportionally more energy than any other tissue in the body, so it has to have a good supply of blood. However, with ageing the high energy demand produces debris and there is progressive inflammation even in normal animals. In humans this can result in a decline of up to 30% in the numbers of light receptive cells in the eye by the time we are 70 and so lead to poorer vision."

We need cell therapies to replace tired eye blood vessels, rod cells, cone cells, and other retinal cells. The inflammation and decline in number of light receptive cells with age could be reversed and some day will be reserved. Faster please, as Glenn Reynolds likes to say.

The vitamin D reduced both inflammation and amyloid beta.

The researchers found that when old mice were given vitamin D for just six weeks, inflammation was reduced, the debris partially removed, and tests showed that their vision was improved.

The researchers identified two changes taking place in the eyes of the mice that they think accounted for this improvement. Firstly, the number of potentially damaging cells, called macrophages, were reduced considerably in the eyes of the mice given vitamin D. Macrophages are an important component of our immune systems where they work to fight off infections. However in combating threats to the aged body they can sometimes bring about damage and inflammation. Giving mice vitamin D not only led to reduced numbers of macrophages in the eye, but also triggered the remaining macrophages to change to a different configuration. Rather than damaging the eye the researchers think that in their new configuration macrophages actively worked to reduce inflammation and clear up debris.

The second change the researchers saw in the eyes of mice given vitamin D was a reduction in deposits of a toxic molecule called amyloid beta that accumulates with age. Inflammation and the accumulation of amyloid beta are known to contribute, in humans, to an increased risk of age-related macular degeneration (AMD), the largest cause of blindness in people over 50 in the developed world. The researchers think that, based on their findings in mice, giving vitamin D supplements to people who are at risk of AMD might be a simple way of helping to prevent the disease.

This result is consistent with earlier research on humans that found that higher blood vitamin D levels are associated with a lower risk of age-related macular degeneration. Also, higher vitamin D is associated with healthier blood vessels.

Some evidence exists that too much vitamin D increases risk of atrial fibrillation. But the levels associated with healthier blood vessels and lower AMD risk in humans are below those found to increase atrial fibrillation. So this makes me think there's some value in getting one's vitamin D levels tested and then supplement as necessary to keep one's blood vitamin D in the normal (41-80 ng/dl) range.

People who aren't made poorer by recessions spend less for status signaling when others have to cut back on their own status-driven spending. If others can't flash as many status signals then people feel less need to do their own spending to signal higher status.

"Even when their consumption budget is unaffected by a recession, consumers will change their expenditure patterns because some of these expenses depend on social standards that shift with economic conditions," write authors Wagner A. Kamakura (Duke University) and Rex Yuxing Du (University of Houston).

So a recession allows some people to voluntarily take a breather from status spending.

The authors analyzed U.S. household expenditure data for more than two decades, using a model that allowed them to separate budget and positionality effects. "As one would expect, we find that the share of consumption budget devoted to nonessentials (apparel, jewelry and watches, recreation, traveling) drops, while shares devoted to essentials (food at home, housing, utilities) increase during a recession due to the budget effect," the authors write.

Wealthy consumers don't necessarily spend less out of empathy for those who are less well off. Instead, they perceive a reduction in others' expenditures on positional goods and services and feel they don't need to spend as much to maintain the same status relative to their peers, the authors explain.

During hard times, visible luxuries are hit twice, because people generally have less to spend and those who can consume feel less compelled to show off. "Keeping up with the Joneses is less onerous when they are not keeping up," the authors conclude.

People with a lower instinctive (or even practical) need to flash status symbols are relatively more free to live the way they want to live. I am reminded of a piece that Marty Cortland wrote about 4 years ago on how he had to buy a Lexus because his wife thought they weren't rich enough to drive around in a mere Buick. The tyranny of upper middle classness: you've got to flash status symbols because you aren't known as a billionaire.

“I’m not driving a Buick,” she declared. “There is no way I’m showing up at playgroup at Brook Hollow in a Buick.”

“But what about Ross Perot?” I argued. “He drives a Crown Vic.”

“Ross Perot is a billionaire,” she shrieked. “He can afford to drive anything he wants!”

I bet there are genetic variants that cause different levels of desire to have status. A combination of a low desire for status and a high desire for savings would seem the best combination for a lower stress life. Though one might still feel stress about not having saved enough.

Polysilicon crystal is an input into making silicon-based photovoltaics. After peaking at over $400 per kilogram in 2008 due to rapidly rising demand big capital investments in polysilicon crystal manufacturing plants led to a glut. Now polysilicon crystal has fallen in price by an order of magnitude. The good news: according to that link the manufacturing cost (at least for lower cost producers) is still lower than the market price. So the current lower market price is sustainable and will lead to lower silicon PV prices as new contracts for polysilicon are negotiated.

However, oversupply in the polysilicon market pushed the spot price of silicon down from $80 per kilogram in late March 2011 to under $30 per kilogram in December, representing more than a 60 percent drop.

For the future of silicon PV what we need to know: how much further can polysilicon manufacturing costs drop? Is energy cost the biggest cost in that process? Are we need the floor for long term polysilicon prices? Can silicon PV continue to drop in cost as fast as thin films?

As I've written previously, the manufacturing and installation cost trends are what we should watch when it comes to the future of renewables. Market prices can be going up and down independent of manufacturing costs.

Update: In the comments Ronald Brakels points to a report on research to lower the energy cost of making polysilicon crystals. This has the potential to raise the energy return on energy invested (EROEI) of silicon PV.

At least among the overweight eating carbs that digestly slowly lowers markers for inflammation. Choose your carbohydrates for lower glycemic index.

SEATTLE – Among overweight and obese adults, a diet rich in slowly digested carbohydrates, such as whole grains, legumes and other high-fiber foods, significantly reduces markers of inflammation associated with chronic disease, according to a new study by Fred Hutchinson Cancer Research Center. Such a "low-glycemic-load" diet, which does not cause blood-glucose levels to spike, also increases a hormone that helps regulate the metabolism of fat and sugar. These findings are published online ahead of the February print issue of the Journal of Nutrition.

The controlled, randomized feeding study, which involved 80 healthy Seattle-area men and women – half of normal weight and half overweight or obese – found that among overweight and obese study participants, a low-glycemic-load diet reduced a biomarker of inflammation called C-reactive protein by about 22 percent.

"This finding is important and clinically useful since C-reactive protein is associated with an increased risk for many cancers as well as cardiovascular disease," said lead author Marian Neuhouser, Ph.D., R.D., a member of the Cancer Prevention Program in the Public Health Sciences Division at the Hutchinson Center. "Lowering inflammatory factors is important for reducing a broad range of health risks. Showing that a low-glycemic-load diet can improve health is important for the millions of Americans who are overweight or obese."

The diets had the same amounts of total carbohydrates.

Study participants completed two 28-day feeding periods in random order – one featuring high-glycemic-load carbohydrates, which typically are low-fiber, highly processed carbs such as white sugar, fruit in canned syrup and white flour; and the other featuring low-glycemic-load carbohydrates, which are typically higher in fiber, such as whole-grain breads and cereals. The diets were identical in carbohydrate content, calories and macronutrients. All food was provided by the Hutchinson Center's Human Nutrition Laboratory, and study participants maintained weight and physical activity throughout.

Check out Rick Mendosa's tables on glycemic index and glycemic load. Become familiar with higher glycemic index foods and avoid them.

A third of your gasoline goes toward overcoming friction. Over half of that friction might become avoidable within 15 to 25 years.

No less than one third of a car's fuel consumption is spent in overcoming friction, and this friction loss has a direct impact on both fuel consumption and emissions. However, new technology can reduce friction by anything from 10% to 80% in various components of a car, according to a joint study by VTT Technical Research Centre of Finland and Argonne National Laboratory (ANL) in USA. It should thus be possible to reduce car's fuel consumption and emissions by 18% within the next 5 to 10 years and up to 61% within 15 to 25 years.

There are 612 million cars in the world today. The average car clocks up about 13,000 km per year, and in the meantime burns 340 litres of fuel just to overcome friction, costing the driver EUR 510 per year.

Electric cars lose far less of their energy to friction. So they have less to gain from friction reduction. So reduced friction loss will improve the relative advantage of cars buring liquid hydrocarbon fuels versus electric cars.

Of the energy output of fuel in a car engine, 33% is spent in exhaust, 29% in cooling and 38% in mechanical energy, of which friction losses account for 33% and air resistance for 5%. By comparison, an electric car has only half the friction loss of that of a car with a conventional internal combustion engine.

Annual friction loss in an average car worldwide amounts to 11,860 MJ: of this, 35% is spent in overcoming rolling resistance in the wheels, 35% in the engine itself, 15% in the gearbox and 15% in braking. With current technology, only 21.5% of the energy output of the fuel is used to actually move the car; the rest is wasted.

One thought: on shorter trips it should be possible to avoid the need for a cooling air conditioner and gasoline power lost to it. Imagine when parked you could plug in the car and the electric power would operate a condenser to super cool some liquid. Then that frozen material could provide a source of cooling for, say, an hour or two.

Newer materials can cut friction. But what about the costs?

A recent VTT and ANL study shows that friction in cars can be reduced with new technologies such as new surface coatings, surface textures, lubricant additives, low-viscosity lubricants, ionic liquids and low-friction tyres inflated to pressures higher than normal.

Friction can be reduced by 10% to 50% using new surface technologies such as diamond-like carbon materials and nanocomposites. Laser texturing can be employed to etch a microtopography on the surface of the material to guide the lubricant flow and internal pressures so as to reduce friction by 25% to 50% and fuel consumption by 4%. Ionic liquids are made up of electrically charged molecules that repel one another, enabling a further 25% to 50% reduction in friction.

The payback will come faster in commercial vehicles that travel great distances every year. So are diamond-line carbon materials getting designed into engines or transmissions of any long distance trucks today?

The Norwegian Institute of Public Health says for healthier air light your wood burning heaters from the top, not the bottom. An added benefit: more complete burning means higher efficiency. You get more heat from the wood.

• when the wood is lit from above, the heat radiates to warm the wood underneath. These pieces of wood will begin to emit gases which will rise, meet the flames and ignite
• if you light from below, the heat radiation will cause the wood over the flames to release gases which will rise. Without flames at the top of the wood, the gases will be released unburnt out of the combustion chamber to the chimney, where they will form particles
• the particle emissions from the chimney will be halved
• you gain maximum heating efficiency from your wood and thus lower your heating costs

Before anyone states "this is obvious": I've seen wood fires lit from the bottom many times. It is usually seen as easier to light from the bottom. Kindling can light bigger logs above it.

But it makes sense that a fire on top can burn the gases that get released from warming wood underneath them. So try to light the top.

Update: "pond" points to instructions on how to easily light from the top. What's still missing: How to easily load new logs into a burning fire bottom-up?

Every time most cells divide their telomere chromosome caps get shorter. When the telomere caps get very short cellular division is inhibited. Cells that can't divide can not repair damaged tissue. It is not a coincidence that cells around damaged arthritic joints have short telomeres.

Telomeres, the very ends of chromosomes, become shorter as we age. When a cell divides it first duplicates its DNA and, because the DNA replication machinery fails to get all the way to the end, with each successive cell division a little bit more is missed. New research published in BioMed Central's open access journal Arthritis Research & Therapy shows that cells from osteoarthritic knees have abnormally shortened telomeres and that the percentage of cells with ultra short telomeres increases the closer to the damaged region within the joint.

While the shortening of telomeres is an unavoidable side effect of getting older, telomeres can also shorten as a result of sudden cell damage, including oxidative damage. Abnormally short telomeres have been found in some types of cancer, possibly because of the rapid cell division the cells are forced to undergo.

The question: are the short telomeres a result of osteoarthritis? Or are the short telomeres a cause of osteoarthritis? Does the inflammation associated with osteoarthritis accelerate cell division and thereby cause short telomeres? Or do joints wear down and become osteoarthritic once few cells remain that can do repairs on them?

A Danish team developed a better assay to measure telomere length. Better assays speed up scientific discovery.

There has been some evidence from preliminary work done on cultured cells that the average telomere length is also reduced in osteoarthritis (OA). A team of researchers from Denmark used newly developed technology (Universal single telomere length assay) to look in detail at the telomeres of cells taken from the knees of people who had undergone joint replacement surgery. Their results showed that average telomere length was, as expected, shortened in OA, but that also 'ultra short' telomeres, thought to be due to oxidative stress, were even more strongly associated with OA.

Maria Harbo who led this research explained, "We see both a reduced mean telomere length and an increase in the number of cells with ultra short telomeres associated with increased severity of OA, proximity to the most damaged section of the joint, and with senescence. Senescence can be most simply explained as biological aging and senescent cartilage within joints is unable to repair itself properly."

Cartilage damage and telomere shortening are both contributing to the development of osteoarthritis.

She continued, "The telomere story shows us that there are, in theory, two processes going on in OA. Age-related shortening of telomeres, which leads to the inability of cells to continue dividing and so to cell senescence, and ultra short telomeres, probably caused by compression stress during use, which lead to senescence and failure of the joint to repair itself. We believe the second situation to be the most important in OA. The damaged cartilage could add to the mechanical stress within the joint and so cause a feedback cycle driving the progression of the disease."

Lots of researchers investigate a large assortment of diseases of old age. But many of these diseases have a common cause: loss of ability of the body to do repairs. So while the diseases manifest in different ways with different symptoms they could be reversed with a common strategy: restore the body's ability to do repairs on itself. Cell therapies to deliver youthful cells are a key part of a larger strategy to reverse the aging process and repair aged tissues.